Permissive hypofiltration

Lakhmir S Chawla,Claudio Ronco,John A Kellum

doi:10.1186/cc11253

Abstract

Acute kidney injury (AKI) is a syndrome with a multitude of causes and is associated with high mortality and a permanent loss of renal function. Our current understanding of the most common causes of AKI is limited, and thus a silver bullet therapy remains elusive. A change in the approach to AKI that shifts away from the primary composite endpoint of death/dialysis, and instead focuses on improving survival and mitigating permanent renal damage, is likely to be more fruitful. We suggest that the current approach of augmenting renal function by increasing the renal blood flow or glomerular filtration rate during AKI may actually worsen outcomes. Analogous to the approach towards adult respiratory distress syndrome that limits ventilator-induced lung injury, we propose the concept of permissive hypofiltration. The primary goals of this approach are: resting the kidney by providing early renal replacement therapy, avoiding the potentially injurious adverse events that occur during AKI (for example, fluid overload, hypophosphatemia, hypothermia, and so forth), and initiating therapies focused on improving survival and mitigating permanent loss of kidney function.

Highlights

Acute kidney injury (AKI) is a disorder that often complicates the hospital course of patients and is associated with a significant mortality risk. ose patients with the most severe forms of AKI, who develop such significant solute or fluid imbalance that they are usually treated with renal replacement therapy (RRT), experience a hospital mortality of approximately 60% [1]
Available preclinical and human data suggest that septic-associated AKI is not associated with tubular necrosis [5,6]. ese same studies demonstrate that renal blood flow (RBF) in sepsis is typically increased, and that, despite this augmented RBF, septic patients still experience a drop in glomerular filtration rate (GFR) and develop AKI
The few studies that have assessed histopathology in septic patients do not show evidence of tubular necrosis [7]. e failure to develop appropriate therapeutic agents for AKI may be due to the fact that the therapeutic agents being considered work via increasing the GFR by increasing RBF – which is unlikely to benefit those patients with sepsis, the most common exposure associated with AKI

Summary

Introduction

Acute kidney injury (AKI) is a disorder that often complicates the hospital course of patients and is associated with a significant mortality risk. ose patients with the most severe forms of AKI, who develop such significant solute or fluid imbalance that they are usually treated with renal replacement therapy (RRT), experience a hospital mortality of approximately 60% [1]. Both have multiple etiologies; and the most common cause for both ARDS and AKI is sepsis Both syndromes are associated with increased mortality; and both affect critically ill patients, contributing to an increased risk of death. As in the example of myocardial infarction and ARDS, organ support during injury is a key approach to improving outcomes Consistent with this concept, early institution of RRT has the capacity to rest the injured organ by limiting the solute load and mitigating fluid overload. The third theme is based on recognizing that thermal control, antibiotic dosing and maintenance of electrolyte and volume balance must be carried out carefully during RRT to avoid harm This is one of the core lessons from the experience of ARDS therapy; limiting the harm of the device–patient interaction. The goal of the therapeutic agent would be to decrease mortality, enhance renal recovery and decrease the incidence of long-term loss of renal

Any history of renal allograft

Conclusion

Findings

34. Lowe KG